Hypoxic Ischemic Encephalopathy - Oren Zarif - Hypoxic Ischemic Encephalopathy
Hypoxic ischemic encephalopathy, also known as HIE, is a condition that occurs when a brain is deprived of oxygen. Survivors may experience brain damage and neurological delays. Some patients may develop cerebral palsy or epilepsy, among other problems.
Although there is no clear definition for HIE, it is graded according to clinical examination, Sarnat staging, and Thompson Score. Neuroimaging can also provide important information.
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The final degree of neuronal damage in HIE depends on the nature and extent of the initial insult, as well as the subsequent effect of reperfusion injury and apoptosis. The biochemical events that occur in the brain after hypoxic-ischemic injury vary, but are likely related. Although the precise mechanism is not known, recent studies have suggested that inflammatory mediators play a role in the progression of HIE.
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The definition of hypoxic ischemic encephalopathies is quite wide. One of them, neonatal HIE, is one of the most common causes of newborn brain damage. Other causes of neonatal encephalopathy include infections, certain metabolic disorders, and specific genetic syndromes. The symptoms and diagnosis of HIE vary from child to child. The severity and duration of brain damage depend on the location of the brain that was affected and the length of the deprivation.
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Despite the lack of definitive definitions, the presence of HIE is a serious problem and the risk of permanent disability is high. In children, the consequences of HIE can be devastating: they may develop Cerebral Palsy, mental retardation, and even death. Although the symptoms of HIE may go away on their own after 24 hours, it is critical to monitor the symptoms. If your child has the symptoms of HIE, see a doctor immediately. The condition can be treated and managed effectively.
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The basic patterns of HIE are outlined in the following tables. In term infants, hypoxic ischemic injury is predominantly seen in pontosubicular neuronal areas, and in cerebellar regions. It also affects the white matter of the brain and can be dominant or subclinical. The severity of the hypoxia depends on the infant's age and development at the time of the insult. If the hypotension is severe enough, the infant may sustain significant brain damage, including infarctions in the brain stem, deep gray matter, and cerebral cortex.
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As a result, hypoxic ischemic brain injury (HIBI) is the most common cause of death and long-term neurologic disability after CA. Researchers have described a complex pathophysiologic cascade of events that leads to primary and secondary brain injury. In acute HIBI, cerebral blood flow is abruptly interrupted after a CA and, in severe cases, after a few days, the brain continues to suffer from ischemia. The secondary brain injury occurs hours or days after reperfusion and is related to a wide range of factors, including impaired cerebral autoregulation and microcirculatory dysfunction.
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If left untreated, severe HIE can cause long-term disability and may even lead to epilepsy or cerebral palsy in older children. Although a small percentage of newborns are able to survive HIE, the condition is usually permanent and will affect the child's growth. The brain can become damaged permanently and can cause severe impairment in the child's mental and physical development. It is critical that doctors understand this condition in newborns.
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A diagnosis of HIE depends on the extent of encephalopathy and the specific areas of brain injury. Mild encephalopathy is associated with normal neurocognitive outcomes, while moderate encephalopathy can lead to poor cognitive outcomes. MRI imaging is helpful for determining the severity of brain damage. In severe cases, injury to the basal ganglia or watershed region may result in isolated cognitive deficits. Once a child reaches school age, ongoing neuropsychological screening will allow early intervention.
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Current therapies for HIE include therapeutic hypothermia and brain cooling. These therapies have been shown to decrease neurologic mortality and reduce morbidity. Therefore, therapeutic hypothermia is now a standard of care at most academic institutions. Several neuroprotective drugs are now entering clinical trials. The goal is to prevent the brain from becoming completely destroyed. There is no cure for HIE, but treatment options are available.